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Sex differences in extracellular and intracellular calcium-mediated vascular reactivity to vasopressin in rat aorta
In rat thoracic aorta, contractile responses to arginine vasopressin are two-fold higher in females than in males. To determine the roles of extracellular and intracellular Ca 2+ in this sexual dimorphism in vascular function, vascular reactivity and Ca 2+ channel function were examined in thoracic...
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Published in: | European journal of pharmacology 1998-11, Vol.361 (2), p.207-216 |
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Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | In rat thoracic aorta, contractile responses to arginine vasopressin are two-fold higher in females than in males. To determine the roles of extracellular and intracellular Ca
2+ in this sexual dimorphism in vascular function, vascular reactivity and Ca
2+ channel function were examined in thoracic aortae of male and female rats. In the presence of diltiazem (10 μM), maximal contraction to vasopressin was reduced to a greater extent in male (65±2%) than in female aortae (38±1%). Maximal contractile responses to KCl and Bay K 8644 were similar in male and female aortae. Sensitivity to KCl was slightly but significantly higher in male than in female aorta; in contrast, sensitivity to Bay K 8644 was nearly three-fold higher in males than in females. Removal of the endothelium enhanced sensitivity to KCl similarly in male and female aortae. In the presence of simvastatin (60 μM; an inhibitor of intracellular Ca
2+ release), reactivity to vasopressin was reduced substantially in female (42±1%) but unaltered in male aortae. Removal of the endothelium enhanced the inhibitory effect of simvastatin in both female (73±2%) and male aortae (41±2%). These findings demonstrate that male aortae depend more upon extracellular Ca
2+ influx, whereas female aortae depend more upon intracellular Ca
2+ release for vasopressin-induced contraction. |
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ISSN: | 0014-2999 1879-0712 |
DOI: | 10.1016/S0014-2999(98)00700-6 |